Evidence mapPaperPMID 40935652Full record

ReviewDiabetes & metabolism journal2025

Hepatic Insulin Resistance and Steatosis in Metabolic Dysfunction-Associated Steatotic Liver Disease: New Insights into Mechanisms and Clinical Implications.

Xuan Trong Truong, Dae Ho Lee

Abstract readReview
In one paragraph

Review in Diabetes & metabolism journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Unrevealing the Role of Flavonoids in Mitigation of Non-Alcoholic Fatty Liver Disease.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
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  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Observational
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
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  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Xuan Trong TruongDepartment of Genome Medicine and Science, Gachon University College of Medicine, Incheon, Korea.
Dae Ho LeeDepartment of Internal Medicine, Gachon University Gil Medical Center, Gachon University College of Medicine, Incheon, Korea.

Funding

Gachon University GCU-202309080001Gachon University GCU-20240928000
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) represents a progressive spectrum ranging from simple hepatic steatosis to steatohepatitis and fibrosis. Although insulin resistance (IR) plays a central role in metabolic diseases, in the liver, insulin- or substrate-driven de novo lipogenesis (DNL) promotes triglyceride accumulation through multiple complex regulatory mechanisms, including specific transcription factors, regardless of whether IR is primary or not. Elevated free fatty acids, resulting from increased adipose lipolysis, further augment hepatic lipid storage and contribute to IR and the progression of MASLD through lipotoxic intermediates such as diacylglycerols and ceramides, as well as other pathways. Numerous studies have identified DNL as a major, yet modifiable, contributor to MASLD. In addition, zonal differences in hepatic insulin signaling, non-classical insulin signaling pathways, and activation of the mechanistic target of rapamycin complex 1 and protein kinase C pathways appear to be involved in the development of selective hepatic IR. Recently, new pharmacologic agents, including resmetirom, have shown promise in improving steatohepatitis and fibrosis in MASLD. Nevertheless, sustained weight loss through lifestyle modification remains the cornerstone of MASLD prevention and therapy. Further mechanistic understanding of how IR and substrate overload promote DNL and hepatic fat accumulation is critical for developing effective treatments for MASLD.

Indexed as

Fatty LiverInsulin ResistanceLiverAnimalsHumansLipogenesisSignal TransductionFatty acids, nonesterifiedInsulin resistanceLipogenesisNon-alcoholic fatty liver disease

Identifiers

PMID40935652
PMCPMC12436041

What Socratic holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.